Quiflapon-sodium-MK591-DataSheet-生命科学试剂-MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEQuiflapon sodiumCat. No.: HY-50714CAS No.: 147030-01-1Synonyms: MK591分式: CHClNNaOS分量: 609.15作靶点: FLAP作通路: Immunology/Inflammation储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性数据体外实验 DMSO : 50 mg/mL (82

2、.08 mM; Need ultrasonic)H2O : 40% PEG300 5% Tween-80 45% salineSolubility: 2.75 mg/mL (4.51 mM); Clear solution2. 请依序添加每种溶剂： 10% DMSO 90% corn oilSolubility: 2.75 mg/mL (4.51 mM); Clear solution1/3 Master of Small Molecules 您边的抑制剂师www.MedChemEBIOLOGICAL ACTIVITY物活性 Quiflapon sodium (MK591)是选择性的，特异性的

3、 FLAP 抑制剂。体外研究 Quiflapon sodium (MK591) and SB203580 are able to block SEB-induced human PBMC cell proliferation.Quiflapon sodium (MK591) down regulates three genes for cathepsin L, IL-17 and guanylate binding protein(GBP)-2 that are up regulated by SEB 1. Quiflapon sodium (MK591) undergoes apoptosi

4、s within hours oftreatment. Quiflapon sodium (MK591) also induces rapid activation of the stress kinase, c-Jun N-terminalkinase (JNK), which plays an important role in the apoptosis process. Quiflapon sodium (MK591) triggersapoptosis in prostate cancer cells without inhibition of PI3K-Akt, or ERK. M

5、oreover, MK591 and LY294002(an inhibitor of PI3K) exert synergistic effect in inducing apoptosis in prostate cancer cells 2. Quiflaponsodium (MK591) influences cAMP response element-binding protein but not Sp1 4.体内研究 Hyperoxia groups of mice treated with Quiflapon sodium (MK591) (20, 40 mg/kg) show

6、alveolarization thatresembles that of room air controls while untreated hyperoxia groups show definite evidence of aberrantalveolarization but no inflammation 3. Comparison of the A-immunopositive areas between the placeboand Quiflapon sodium (MK591) (320 mg/kg)-treated group reveals a statistically

7、 significant reduction of theamyloid burden in the treated mice. Quiflapon sodium (MK591) also has a significant reduction in brain levelsof IL-1. Mice treated with Quiflapon sodium (MK591) show a statistically significant decrease in the steady-state levels of total CREB and its phosphorylated form

8、 at Ser133 4.PROTOCOLKinase Assay 2 LNCaP cells (appr 3105) are plated and treated with inhibitors or solvent vehicle for varying periods of time.Then the cells are lysed in lysis buffer containing 0.2% CHAPS detergent plus protease and phosphataseinhibitors, and the enzymatic activity of Akt is mea

9、sured by a kit following methods supplied by themanufacturer.MCE has not independently confirmed the accuracy of these methods. They are for reference only.Animal The Tg2576 transgenic mice expressing human APP with the Swedish mutation (K670N/M671L) are used inAdministration 4 these studies. They a

10、re genotyped by PCR analysis using tail DNA and kept in a pathogen-free environment,on a 12-hour light/dark cycle and have access to food and water ad libitum. All the experiments presented inthis paper are performed with female mice. Starting at 7 months of age, mice are randomized to receive MK-59

11、1 (40 mg/kg weight) (n=11) or vehicle (n=9) in their chow diet for 8 months until they are 15 months old.Considering that each mouse eats on average 5 g/day of chow diet and the diet is formulated for 320 mgQuiflapon sodium (MK591) per kg diet, the final dose of the active drug is approximately 40 m

12、g/kgweight/day. During the study, mice in both groups gain weight regularly, and no significant difference inweight is detected between the two groups. No macroscopic effect on the overall general health is observedin the animals receiving the active treatment. Post-mortem examination shows no sign

13、of macroscopicpathology in any of the organs considered (spleen, liver, thymus, ileum).MCE has not independently confirmed the accuracy of these methods. They are for reference only.REFERENCES2/3 Master of Small Molecules 您边的抑制剂师www.MedChemE1. Mendis C, et al. Effect of 5-lipoxygenase inhibitor MK59

14、1 on early molecular and signaling events induced by staphylococcal enterotoxinB in human peripheral blood mononuclear cells. FEBS J. 2008 Jun;275(12):3088-98.2. Sarveswaran S, et al. MK591, a leukotriene biosynthesis inhibitor, induces apoptosis in prostate cancer cells: synergistic action withLY29

15、4002, an inhibitor of phosphatidylinositol 3-kinase. Cancer Lett. 2010 May 28;291(2):167-76.3. Park MS, et al. 5-Lipoxygenase-activating protein (FLAP) inhibitor MK-0591 prevents aberrant alveolarization in newborn mice exposedto 85% oxygen in a dose- and time-dependent manner. Lung. 2011 Feb;189(1):43-50.4. Chu J, et al. Involvement of 5-lipoxygenase activating protein in the amyloidotic phenotype of an Alzheimers disease mouse model. JNeuro